ACC/AHA/ASE 2003 guideline update for the clinical application of echocardiography

Mechanical ventilation induces cyclic changes in vena cava blood flow, pulmonary artery blood flow, and aortic blood flow. At the bedside, respiratory changes in aortic blood flow are reflected by "swings" in blood pressure whose magnitude is highly dependent on volume status. During the past few years, many studies have demonstrated that arterial pressure variation is neither an indicator of blood volume nor a marker of cardiac preload but a predictor of fluid responsiveness. That is, these studies have demonstrated the value of this physical sign in answering one of the most common clinical questions, Can we use fluid to improve hemodynamics?, while static indicators of cardiac preload (cardiac filling pressures but also cardiac dimensions) are frequently unable to correctly answer this crucial question. The reliable analysis of respiratory changes in arterial pressure is possible in most patients undergoing surgery and in critically ill patients who are sedated and mechanically ventilated with conventional tidal volumes.

Changes in arterial pressure during mechanical ventilation.

A 62-year-old man presents with a three-day history of progressive dyspnea, nonproductive cough, and low-grade fever. His blood pressure is 100/60 mm Hg, his heart rate 110 beats per minute, his temperature 37.9°C, and his oxygen saturation while breathing room air 86 percent. Chest auscultation reveals rales and rhonchi bilaterally. A chest radiograph shows bilateral pulmonary infiltrates consistent with pulmonary edema and borderline enlargement of the cardiac silhouette. How should this patient be evaluated to establish the cause of the acute pulmonary edema and to determine appropriate therapy?

/pdf/clinical-practice-acute-pulmonary-edema-198tg0zcc1.pdf

Clinical practice. Acute pulmonary edema.

Since its introduction into the operating room in the early 1980s, transesophageal echocardiography (TEE) has gained widespread use during cardiac, major vascular, and transplantation surgery, as well as in emergency and intensive care medicine. Moreover, TEE has become an invaluable diagnostic tool for the management of patients with cardiovascular disease in a nonoperative setting. In comparison with other diagnostic modalities, TEE is relatively safe and noninvasive. However, the insertion and manipulation of the ultrasound probe can cause oropharyngeal, esophageal, or gastric trauma. Here, the authors review the safety profile of TEE by identifying complications and propose a set of relative and absolute contraindications to probe placement. In addition, alternative echocardiographic modalities (e.g., epicardial echocardiography) that may be considered when TEE probe placement is contraindicated or not feasible are discussed.

http://swissecho.ch/en/documents/12_Guidelines_TEE_safety_JASE_2010.pdf

Safety of Transesophageal Echocardiography

Background: Cardiac depression in severe sepsis and septic shock is characterized by left ventricular (LV) failure. To date, it is unclear whether clinically unrecognized myocardial cell injury accompanies, causes, or results from this decreased cardiac performance. We therefore studied the relationship between cardiac troponin I (cTnI) and T (cTnT) and LV dysfunction in early septic shock.

Methods: Forty-six patients were consecutively enrolled, fluid-resuscitated, and treated with catecholamines. Cardiac markers were measured at study entry and after 24 and 48 h. LV function was assessed by two-dimensional transesophageal echocardiography.

Results: Increased plasma concentrations of cTnI (≥0.4 μg/L) and cTnT (≥0.1 μg/L) were found in 50% and 36%, respectively, of the patients at one or more time points. cTnI and cTnT were significantly correlated ( r = 0.847; P <0.0001). Compared with cTnI-negative patients, cTnI-positive subjects were older, presented higher Acute Physiology and Chronic Health Evaluation II scores at diagnosis, and tended to have a worse survival rate and a more frequent history of arterial hypertension or previous myocardial infarction. In contrast, the two groups did not differ in type of infection or pathogen, or in dose and type of catecholamine administered. Continuous electrocardiographic monitoring in all patients and autopsy in 12 nonsurvivors did not disclose the occurrence of acute ischemia during the first 48 h of observation. LV dysfunction was strongly associated with cTnI positivity (78% vs 9% in cTnI-negative patients; P <0.001). In multiple regression analysis, both cTnI and cTnT were exclusively associated with LV dysfunction ( P <0.0001).

Conclusions: These findings suggest that in septic shock, clinically unrecognized myocardial cell injury is a marker of LV dysfunction. The latter condition tends to occur more often in severely ill older patients with underlying cardiovascular disease. Further studies are needed to determine the extent to which myocardial damage is a cause or a consequence of LV dysfunction.

Cardiac Troponins I and T Are Biological Markers of Left Ventricular Dysfunction in Septic Shock

Evaluation of Transesophageal Echocardiography as a Diagnostic and Therapeutic Aid in a Critical Care Setting

Acute Hemodynamic Changes of Pressure-controlled Inverse Ratio Ventilation in the Adult Respiratory Distress Syndrome: A Transesophageal Echocardiographic and Doppler Study

Transesophageal Echo-doppler evaluation of the hemodynamic effects of positive-pressure ventilation after coronary artery surgery.

Doppler evaluation of right ventricular outflow impedance during positive-pressure ventilation☆

Cardiovascular hemodynamics were studied noninvasively before, during and after hemodialysis with ultrafiltration in 18 patients on chronic hemodialysis. The cardiac output (CO) was determined by a continuous wave Doppler method. Overall, no major CO changes were seen (7.8 +/- 0.6 l/min post- versus 7.4 +/- 0.5 l/min pre-dialysis). Mean blood pressure rose slightly but significantly from 103 +/- 4 mmHg before to 113 +/- 3 mmHg after hemodialysis (p less than 0.01). Important interindividual differences in the intradialytic evolution of CO were observed. In patients with previous myocardial infarction or dilated cardiomyopathy (n = 12), CO rose significantly from 7.3 +/- 0.7 l/min before to 8.4 +/- 0.6 l/min after hemodialysis (p less than 0.05), while in patients without manifest myocardial disease (n = 6) CO decreased from 7.5 +/- 0.7 l/min to 6.6 +/- 0.9 l/min (NS). Comparison of the evolution of CO in both groups by variance analysis revealed a significant difference (p less than 0.01). It is concluded that, in response to hemodialysis with ultrafiltration, CO probably will increase in patients with myocardial infarction or congestive cardiomyopathy, but probably will decrease in patients without.

J Everaert

Papers

Evaluation of Transesophageal Echocardiography as a Diagnostic and Therapeutic Aid in a Critical Care Setting

Acute Hemodynamic Changes of Pressure-controlled Inverse Ratio Ventilation in the Adult Respiratory Distress Syndrome: A Transesophageal Echocardiographic and Doppler Study

Transesophageal Echo-doppler evaluation of the hemodynamic effects of positive-pressure ventilation after coronary artery surgery.

Doppler evaluation of right ventricular outflow impedance during positive-pressure ventilation☆

Cardiac output-changes during hemodialysis with ultrafiltration.